Long-Term Outcome after Vitrectomy for Macular Edema with Retinal Vein Occlusion Dividing into the Occlusion Site

Purpose. To investigate the efficacy of treatment for macular edema secondary to retinal vein occlusion (RVO) with vitrectomy. Methods. This retrospective study identified patients with macular edema associated with RVO between January 2004 and April 2006. Inclusion criteria were eyes with (1) preoperative visual acuity (VA) of 20/40 or worse, (2) a central foveal thickness (CFT) greater than 250 μm, and (3) vitrectomy with internal limiting membrane and intravitreal triamcinolone acetonide. Each patient had their RVO classified as a major or macular BRVO or hemispheric RVO (HSRVO). Results. Forty-six eyes with major BRVO, 18 eyes with macular BRVO, and 17 eyes with HSRVO were investigated. VA was significantly improved at 24 months after surgery for each group (P<0.05). Vision in the macular BRVO group 24 months after surgery was significantly better than that in other groups (P<0.05). For each group, a concomitant reduction of CFT was noted at every time point when compared to preoperative values (P<0.001). Conclusions. In macular BRVO, the postoperative vision 24 months after surgery was significantly better than the other groups. These findings suggest that additional and earlier treatments might be more important for patients with major BRVO and HSRVO than for those with macular BRVO

Overexpression of SOD in retina: Need for increase in H2O2-detoxifying enzyme in same cellular compartment

In retinitis pigmentosa (RP), various mutations cause rod photoreceptor cell death leading to increased oxygen levels in the outer retina, progressive oxidative damage to cones, and gradual loss of cone cell function. We have been exploring the potential of overexpressing components of the endogenous antioxidant defense system to preserve cone cell function in rd10+/+ mice, a model of RP. Rd10+/+ mice deficient in superoxide dismutase 1 (SOD1) showed increased levels of superoxide radicals and carbonyl adducts (a marker of oxidative damage) in the retina, and more rapid loss of cone function than rd10+/+ mice with normal levels of SOD1. This suggests that SOD1 is an important component of the antioxidant defense system of cones, but increased expression of SOD1 in rd10+/+ mice increased oxidative damage and accelerated the loss of cone function. Co-expression of SOD1 with glutathione peroxidase 4 (Gpx4), which like SOD1 is localized in the cytoplasm, but not with catalase targeted to the mitochondria, reduced oxidative damage in the retina and significantly slowed the loss of cone cell function in rd10+/+ mice. Gene transfer resulting in increased expression of SOD2, but not co-expression of SOD2 and mitochondrial Gpx4, resulted in high levels of H2O2 in the retina. These data suggest that in order to provide benefit in RP, over-expression of a SOD must be combined with expression of a peroxide detoxifying enzyme in the same cellular compartment

Increased Expression of Catalase and Superoxide Dismutase 2 Reduces Cone Cell Death in Retinitis Pigmentosa

Oxidative and nitrosative damage are major contributors to cone cell death in retinitis pigmentosa (RP). In this study, we explored the effects of augmenting components of the endogenous antioxidant defense system in models of RP, rd1, and rd10 mice. Unexpectedly, overexpression of superoxide dismutase 1 (SOD1) in rd1 mice increased oxidative damage and accelerated cone cell death. With an elaborate mating scheme, genetically engineered rd10 mice with either inducible expression of SOD2, Catalase, or both in photoreceptor mitochondria were generated. Littermates with the same genetic background that did not have increased expression of SOD2 nor Catalase provided ideal controls. Coexpression of SOD2 and Catalase, but not either alone, significantly reduced oxidative damage in the retinas of postnatal day (P) 50 rd10 mice as measured by protein carbonyl content. Cone density was significantly greater in P50 rd10 mice with coexpression of SOD2 and Catalase together than rd10 mice that expressed SOD2 or Catalase alone, or expressed neither. Coexpression of SOD2 and Catalase in rd10 mice did not slow rod cell death. These data support the concept of bolstering the endogenous antioxidant defense system as a gene-based treatment strategy for RP, and also indicate that coexpression of multiple components may be needed